Dissecting the role of mineralocorticoid receptors in binge-like alcohol drinking in mice: Finerenone as a potential pharmacotherapy

剖析盐皮质激素受体在小鼠暴饮行为中的作用:非奈利酮作为一种潜在的药物疗法

阅读:1

Abstract

RATIONALE: Alcohol use disorder (AUD) is a serious public health issue, for which only few pharmacological treatments are currently available. The mineralocorticoid receptor (MR) has been investigated as a potential pharmacotherapeutic target for AUD. Treatment with the prototypical MR antagonist spironolactone has been associated with a reduction of alcohol consumption in rodents and humans. However, spironolactone is a nonselective MR antagonist and has additional activity on other systems, such as androgen and progesterone receptors. OBJECTIVES: The present study investigated the specific role of MR in modulating alcohol drinking. We tested the effect of selective MR antagonists (finerenone, eplerenone, and PF-03882845), spironolactone’s active metabolites with MR antagonism properties (7α-thiomethylspironolactone [7αTMS] and canrenone), selective MR agonists (aldosterone and fludrocortisone), an androgen receptor antagonist (darolutamide), and a progesterone receptor agonist (dydrogesterone) in a drinking-in-the-dark mouse model of binge-like drinking. RESULTS: We found that finerenone, eplerenone, and PF-03882845 reduced alcohol intake in both male and female mice, whereas 7αTMS, canrenone, aldosterone, fludrocortisone, darolutamide, and dydrogesterone had no effect. Eplerenone and PF-03882845 but not finerenone also reduced the intake of a sweet solution without alcohol, and eplerenone impaired motor coordination. CONCLUSIONS: These results suggest that MRs but not androgen or progesterone receptors are involved in binge-like alcohol drinking, with finerenone as the most selective and effective MR antagonist in reducing alcohol intake. Our findings support the development of clinical trials with finerenone to evaluate its potential therapeutic effects for AUD.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。